File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Different cell kinetic changes in rat stomach cancer after treatment with celecoxib or indomethacin: Implications on chemoprevention

TitleDifferent cell kinetic changes in rat stomach cancer after treatment with celecoxib or indomethacin: Implications on chemoprevention
Authors
Issue Date2005
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htm
Citation
World Journal Of Gastroenterology, 2005, v. 11 n. 1, p. 41-45 How to Cite?
AbstractAim: Mechanisms underlying the chemopreventive effects of cyclooxygenase (COX) inhibitors remain elusive. We have previously shown that celecoxib but not indomethacin could prevent carcinogen-induced gastric cancer development in Wistar rats. This chemopreventive effect appeared to be independent of COX-2 and prostaglandin (PG) E2 suppression since the lowest PGE2 was obtained in indomethacin group. This study compared the cell kinetic changes in stomachs of rats after treatment with celecoxib (5, 10, 20 mg/(kg·d)) or indomethacin (3 mg/(kg·d)) to gain more insights into the chemopreventive mechanism. Methods: The apoptosis and proliferation indexes in gastric tumor, adjacent non-cancer tissues and normal gastric tissues were determined. Apoptosis was quantified by apoptotic nuclei counting and TUNEL, whereas proliferation was determined by Ki67 immunostaining. Results: Treatment with either celecoxib or indomethacin inhibited gastric tumor proliferation by more than 65% (P<0.02). However, celecoxib caused a dose-dependent increase in apoptosis (P<0.05) which was not seen in indomethacin-treated tumors (P = 0.54). The highest apoptosis to proliferation ratio was seen in tumors treated with celecoxib at 10 mg/(kg·d). Treatment with this dose of celecoxib was associated with the lowest incidence of gastric cancer development. Conclusion: Our findings suggest that the difference in chemopreventive effects of indomethacin and celecoxib in this animal model of gastric carcinogenesis is largely due to the differential cell kinetic changes, which does not correlate with the degree of COX-2 and PG suppression. © 2005 The WJG Press and Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162849
ISSN
2015 Impact Factor: 2.787
2015 SCImago Journal Rankings: 1.076
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, Jen_US
dc.contributor.authorTang, BDen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorBai, AHCen_US
dc.contributor.authorZeng, ZRen_US
dc.contributor.authorMa, PKen_US
dc.contributor.authorGo, MYYen_US
dc.contributor.authorHu, PJen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:24:21Z-
dc.date.available2012-09-05T05:24:21Z-
dc.date.issued2005en_US
dc.identifier.citationWorld Journal Of Gastroenterology, 2005, v. 11 n. 1, p. 41-45en_US
dc.identifier.issn1007-9327en_US
dc.identifier.urihttp://hdl.handle.net/10722/162849-
dc.description.abstractAim: Mechanisms underlying the chemopreventive effects of cyclooxygenase (COX) inhibitors remain elusive. We have previously shown that celecoxib but not indomethacin could prevent carcinogen-induced gastric cancer development in Wistar rats. This chemopreventive effect appeared to be independent of COX-2 and prostaglandin (PG) E2 suppression since the lowest PGE2 was obtained in indomethacin group. This study compared the cell kinetic changes in stomachs of rats after treatment with celecoxib (5, 10, 20 mg/(kg·d)) or indomethacin (3 mg/(kg·d)) to gain more insights into the chemopreventive mechanism. Methods: The apoptosis and proliferation indexes in gastric tumor, adjacent non-cancer tissues and normal gastric tissues were determined. Apoptosis was quantified by apoptotic nuclei counting and TUNEL, whereas proliferation was determined by Ki67 immunostaining. Results: Treatment with either celecoxib or indomethacin inhibited gastric tumor proliferation by more than 65% (P<0.02). However, celecoxib caused a dose-dependent increase in apoptosis (P<0.05) which was not seen in indomethacin-treated tumors (P = 0.54). The highest apoptosis to proliferation ratio was seen in tumors treated with celecoxib at 10 mg/(kg·d). Treatment with this dose of celecoxib was associated with the lowest incidence of gastric cancer development. Conclusion: Our findings suggest that the difference in chemopreventive effects of indomethacin and celecoxib in this animal model of gastric carcinogenesis is largely due to the differential cell kinetic changes, which does not correlate with the degree of COX-2 and PG suppression. © 2005 The WJG Press and Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htmen_US
dc.relation.ispartofWorld Journal of Gastroenterologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAdenocarcinoma - Pathology - Prevention & Controlen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshCyclooxygenase 2 Inhibitorsen_US
dc.subject.meshCyclooxygenase Inhibitors - Pharmacologyen_US
dc.subject.meshEpithelial Cells - Drug Effects - Enzymology - Pathologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsoenzymes - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Metabolismen_US
dc.subject.meshPyrazoles - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshStomach Neoplasms - Pathology - Prevention & Controlen_US
dc.subject.meshSulfonamides - Pharmacologyen_US
dc.titleDifferent cell kinetic changes in rat stomach cancer after treatment with celecoxib or indomethacin: Implications on chemopreventionen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.3748/wjg.v11.i1.41-
dc.identifier.pmid15609394-
dc.identifier.pmcidPMC4205381-
dc.identifier.scopuseid_2-s2.0-19944429554en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19944429554&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue1en_US
dc.identifier.spage41en_US
dc.identifier.epage45en_US
dc.identifier.isiWOS:000208097900008-
dc.publisher.placeChinaen_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridTang, BD=7402560876en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridBai, AHC=7006523130en_US
dc.identifier.scopusauthoridZeng, ZR=7402647305en_US
dc.identifier.scopusauthoridMa, PK=18836911500en_US
dc.identifier.scopusauthoridGo, MYY=7101882939en_US
dc.identifier.scopusauthoridHu, PJ=7201989582en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats